Abstract
The infection of bacterial organisms generally causes cell death to facilitate microbial invasion and immune escape, both of which are involved in the pathogenesis of infectious diseases. In addition to the intercellular infectious processes, pathogen-produced/secreted enterotoxins (mostly exotoxins) are the major weapons that kill host cells and cause diseases by inducing different types of cell death, particularly apoptosis and necrosis. Blocking these enterotoxins with synthetic drugs and vaccines is important for treating patients with infectious diseases. Studies of enterotoxin-induced apoptotic and necrotic mechanisms have helped us to create efficient strategies to use against these well-characterized cytopathic toxins. In this article, we review the induction of the different types of cell death from various bacterial enterotoxins, such as staphylococcal enterotoxin B, staphylococcal alpha-toxin, Panton-Valentine leukocidin, alpha-hemolysin of Escherichia coli, Shiga toxins, cytotoxic necrotizing factor 1, heat-labile enterotoxins, and the cholera toxin, Vibrio cholerae. In addition, necrosis caused by pore-forming toxins, apoptotic signaling through cross-talk pathways involving mitochondrial damage, endoplasmic reticulum stress, and lysosomal injury is discussed.
Highlights
IntroductionPatients with bacteremia may develop moderate or severe sepsis or life-threatening septic shock following multiple organ failure or multiple organ dysfunction syndrome (MOF/MODS) [1,2,3]
Patients with bacteremia may develop moderate or severe sepsis or life-threatening septic shock following multiple organ failure or multiple organ dysfunction syndrome (MOF/MODS) [1,2,3].Patients with MOF/MODS have a 25–50% higher mortality rate than those without MOF/MODS [4,5]. a variety of strategies for managing sepsis have been developed [3,6], it is difficult to prevent because of its complex pathogenic mechanisms, which generally involve severe inflammation and cell death
Enterotoxins chromosomally encoded exotoxins that are originally defined by their cytopathic effects are generally produced from pathogenic bacterial organisms, such as Escherichia coli (E. coli) (alpha-hemolysin (HlyA), Shiga toxins (Stxs), cytotoxic necrotizing factors 1 (CNF1), heat-labile enterotoxins (LT))[7,8], Staphylococcus aureus (S. aureus)(staphylococcal enterotoxins B
Summary
Patients with bacteremia may develop moderate or severe sepsis or life-threatening septic shock following multiple organ failure or multiple organ dysfunction syndrome (MOF/MODS) [1,2,3]. In addition to inflammatory activation, these enterotoxins are cytopathic to host cells through lytic or non-lytic mechanisms by inducing necrosis or apoptosis, respectively. Cytopathic studies have shown that several enterotoxins, including hemolysin, staphylococcal alpha-toxin, pneumolysin, and streptolysin-O, usually cause cell death by altering the apical membrane permeability of the targeting cells [7]. These cytopathic enterotoxins are pore-forming toxins (PFTs), defined as cytolysins. The generation of hydrophilic transmembrane pores, which induces necrotic lysis or permeabilization of host cells or intracellular organelles during infection, is pathogenic for disease development via the disruption of infected tissues/cells and the induction of local and/or systemic immunosuppression. Somatic cell death and immune cell death are required for bacterial invasion and immune escape, respectively
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